C h a p t e r 4 6
Disorders of Skin Integrity and Function
1167
Skin Disorders Due to
Ultraviolet Radiation, Heat,
and Pressure Injury
The skin is highly vulnerable to injury from excessive
ultraviolet (UV) radiation, heat, and unrelieved pressure.
Ultraviolet Radiation
Sunlight is composed of a continuous spectrum of elec-
tromagnetic radiation that is divided into three main
parts or wavelengths: ultraviolet (UV), visible, and
infrared. The UV light region occurs between 100 and
400 nm (nm: one billionth of a meter).
45
Long-wave
UVA radiation is 320 to 400 nm; medium-wave UVB is
280 to 320 nm; and short-wave UVC is 100 to 280 nm.
The ozone layer effectively absorbs UV radiation up
to 310 nm, absorbing all of UVC and much of UVB
radiation. However, damage to the protective ozone
layer is allowing an increased amount of UVB to reach
the earth. The ozone layer does not absorb UVA.
Ultraviolet Radiation Skin Damage
UVA makes up more than 95% of the solar radiation
that reaches us. Compared to UVB, this long-wave radi-
ation penetrates deep into the dermis of the skin and
is more effective in producing an immediate tan. UVB
radiation is a minor but more active constituent of sun-
light. It is more genotoxic and about 1000 times more
capable of causing sunburn than UVA light.
45
UVB acts
mainly on the cells in the basal layer of the epidermis. It
produces direct damage to the DNA and other nuclear
proteins. It also provokes free radical production and
induces a significant reduction in skin antioxidants,
impairing the ability of the skin to protect itself against
damage by the free radicals that are generated.
Etiology and Pathogenesis.
Exposure to UVA and
UVB produces acute effects that are short lived and
reversible. They include erythema, pigmentation, and
injury to Langerhans cells and keratinocytes in the epi-
dermis. These reactions differ depending on whether
the inciting agent is UVA or UVB. For example, UVA-
induced erythema occurs immediately, fades within
hours, and is believed to be due to the “heat load.”
UVB-induced erythema has a delayed response, peaking
within 6 to 24 hours after exposure to sunlight and fad-
ing over 1 or 2 days. Pigmentation or tanning induced
by UVA and UVB is due to increased synthesis of mela-
nin by melanocytes, along with increased transfer of the
melanin to keratinocytes (see Chapter 45). Small doses
of UVA produce transient, immediate darkening of the
skin that fades within 2 hours, whereas higher doses of
UVA can produce pigmentary changes lasting for several
hours to days.
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Tanning induced by UVB is protective
against subsequent exposures, whereas tanning induced
by UVA provides limited protection.
Skin damage induced by UVB is believed to be caused
by the generation of reactive oxygen species and by
damage to melanocytes.
45
Cellular proteins and DNA
are primarily damaged because of their abundance and
ability to absorb UVB radiation. Both UVA and UVB
also deplete Langerhans cells and immune cells. It is
believed that these effects prevent immune cells from
detecting and removing sun-damaged cells with malig-
nant potential. Both UVA and UVB are now considered
causes of skin cancer. UVA may actually be more car-
cinogenic than UVB. Although it causes less sunburn,
UVA is present during all daylight hours, year-round.
Artificial sources of UVA, such as tanning beds and
therapeutic solar interventions (PUVA) for certain skin
conditions, also produce the same effects as solar UVA
in terms of skin cancer. This is of particular concern
because of the increased use of indoor tanning, partic-
ularly among adolescents and young adults who are at
greatest risk of melanoma.
45,46
Educating the popula-
tion about avoiding tanning booths has not increased
compliance; the number of people who use tanning
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Candidal skin infections due to C. albicans occur
most often in persons with diabetes mellitus, those
who are immunosuppressed, or those who have
been treated with broad-spectrum antibiotics.
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Impetigo, which is caused by staphylococci or
β
-hemolytic streptococci, is the most common
superficial bacterial infection.
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Viruses are responsible for verrucae (warts),
herpes simplex type 1 lesions (cold sores or fever
blisters), and herpes zoster (shingles).
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Disorders of the pilosebaceous unit include
acne vulgaris, which is a common skin disorder
of adolescents and young adults that involves
increased sebum production and the presence of
P. acnes; and rosacea, which is a chronic acneform
disorder of middle-aged and older persons.
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Allergic skin responses involve the body’s
immune system and are caused by
hypersensitivity reactions to allergens such
as environmental agents, drugs, and other
substances.They include atopic dermatitis,
urticaria, and drug-induced skin eruptions
(erythema multiforme, Stevens-Johnson
syndrome, and toxic epidermal necrolysis).
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Papulosquamous dermatoses are characterized
by scaling papules and plaques that result
from uncontrolled keratinocyte proliferation.
Psoriasis is a chronic proliferative skin disease
characterized by epidermal hyperplasia. Lichen
planus is a hypersensitivity reaction with
lymphocytic infiltration at the dermal–epithelial
junction.
